LIVER CIRRHOSIS
INTRODUCTION:
Cirrhosis of liver is the end result of the hepatocellular injury characterized by the presence of extensive fibrosis, regenerative nodules and loss of liver architecture.
ETIOLOGY:
A. Viral hepatitis
B. Chronic alcoholism (Laennec’s cirrhosis)
C. Autoimmune hepatitis
D. Drug induced
E. Biliary cirrhosis
F. Hemochromatosis
G. Wilson’s disease
H. Cardiac cirrhosis
I. Alpha-l antitrypsin deficiency
J. Idiopathic
Commonest causes of cirrhosis are viral hepatitis (B, C) and prolonged excessive use of alcohol.
PATHOGENESIS:
l. Irrespective of the cause, the activation of stellate cells is the central event in the development of cirrhosis.
2. The activated stellate cells transform into multifunctional cells upon interaction with hepatocytes, Kupffer cells, and cytokines.
3. The transformed cells form type I collagen leading to fibrosis.
4. The cirrhosis can be micronodular typically in alcoholics where the regenerating nodules are small usually less than 3mm.
5. The macronodular form (more than 3 mm) is characterized by larger nodules and is seen in posthepatitic or postnecrotic cirrhosis.
CLINICAL FEATURES:
l. Cirrhotic patients may be asymptomatic.
2. Mostly symptoms such as weakness, fatigue, weight loss, anorexia, nausea, vomiting and abdominal discomfort occur insidiously.
3. They may be only diagnosed incidentally.
4. Fibrosis and distorted vasculature may lead to portal hypertension and complications associated with it.
5. Patient may present with features of portal hypertension like abdominal distension due to ascites and splenomegaly, haematemesis and melaena due to variceal rupture or hepatic encephalopathy.
6. The liver is firm, nontender, and nodular and is enlarged initially. As the disease progresses, the liver size reduces due to fibrosis.
7. Hepatocellular dysfunction leads to jaundice, oedema, coagulopathy and metabolic abnormalities.
8. Jaundice is generally absent or mild initially. It may become severe at later stages.
9. The signs of chronic hepatic dysfunction such as spider nevi, palmar erythema, gynaecomastia, testicular atrophy and loss of hair may occur due to disturbances in hormonal metabolism.
l0. Females may have loss of libido, menstrual abnormalities and breast atrophy.
l1. Spider nevi are dilated central arterioles with radiating small vessels looking like spider are found mainly on the upper part of the body.
l2. Ascites and hepatic encephalopathy can result from both mechanisms.
l3. Patients may also have haemorrhagic manifestations such as epistaxis and increased menstrual flow.
l4. Other features include enlargement of parotid gland and lacrimal glands, digital clubbing, Dupuytren’s contracture, and skin pigmentation.
Clinical features of cirrhosis may be summarized as follows:
i. Features due to hepatocellular dysfunction include:
Jaundice, ascites, hepatomegaly, spider nevi, palmar erythema, gynaecomastia, testicular atrophy, menstrual abnormalities, breast atrophy, bleeding tendency and hepatic encephalopathy.
ii. Features due to portal hypertension are:
Ascites, splenomegaly, variceal bleeding, and hepatic encephalopathy.
iii. Other miscellaneous features are:
Parotid and lacrimal gland enlargement, clubbing, opaque nails (leukonychia), Dupuytren’s contracture and skin pigmentation.
COMPLICATIONS:
l. Portal hypertension
2. Ascites
3. Upper GI bleeding
4. Spontaneous bacterial peritonitis (SBP)
5. Hepatic encephalopathy
6. Hepatorenal syndrome
7. Hepatocellular carcinoma
LABORATORY FINDINGS:
i. Blood examination:
Anaemia can occur due to bleeding, folate deficiency, marrow suppression or hypesplenism. Leukopenia and thrombocytopenia.
Aminotransferases (ALT, AST) are frequently elevated whereas a rise in the serum bilirubin and ALP may occur later. Serum albumin is low and PT is frequently prolonged.
ii. Imaging:
Ultrasonography to assess the liver size and texture, ascites, portal hypertension and splenomegaly.
iii. Endoscopy:
Upper gastrointestinal endoscopy to detect oesophageal varices and to exclude other causes of upper gastrointestinal bleeding in the stomach and duodenum.
iv. Liver biopsy:
Helps in the assessment of severity of the cirrhotic changes and confirms the specific cause of the cirrhosis.
MANAGEMENT:
It includes general management, treatment of specific cause, management of the complications and liver transplantation.
i. General management:
l. The diet should contain an adequate amount of protein and calories.
2. Vitamin supplementation.
3. Salt restriction is required in case of ascites.
4. Medications which are hepatotoxic or metabolized in liver should be given with caution.
ii. Treatment of specific cause:
l. Alcohol abstinence is mandatory in alcoholic cirrhosis.
2. Specific therapy is needed in hemochromatosis and Wilson’s disease.
iii. Management of specific complications
iv. Liver transplantation:
The irreversible progressive chronic liver failure due to cirrhosis is the most common indication for liver transplantation.
PROGNOSIS:
Overall the prognosis of cirrhosis is poor. The prognosis is favourable if the cause can be corrected.
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